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<p>In this study, the effect of Enoxaparin, a type of low molecular weight heparin (LMWH), on neuronal damage caused by pentylenetetrazol (PTZ)-induced epileptic seizures was investigated. The study utilized C6 and HT-22 cell lines, and the extent to which enoxaparin influenced cytotoxicity in these cells will be evaluated. For this purpose, four groups were established: a control group, a group exposed to PTZ, a group treated with enoxaparin, and a group treated with both PTZ and enoxaparin. Cell viability was measured using a 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2&#xa0;H-tetrazolium-5-carboxanilide (XTT) assay. To evaluate the effects of enoxaparin administration on oxidative stress levels in cell lysates after PTZ-induced neuronal injury, total antioxidant (TAS) and total oxidant (TOS) levels were measured colorimetrically in both cell lines. Mouse nitric oxide (NO), neuronal nitric oxide synthase (nNOS) and rat inducible nitric oxide synthase (iNOS) commercial sandwich ELISA kits were used to measure the effects of enoxaparin on the nitric oxide pathway in cell lysates. As a result of normalization and evaluation of XTT data, it was observed that the viability rate of the group treated with PTZ only decreased to 60% in both cell lines. The results showed that PTZ caused cell damage by increasing oxidative stress and disrupting signaling in neurons. Enoxaparin treatment prevented cytotoxicity by increasing antioxidant capacity and exhibited a neuroprotective effect by suppressing the inflammatory response.</p>

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Investigating the Effect of Low Molecular Weight Heparin, Enoxaparin, on Pentylenetetrazole (PTZ)-Induced Neuronal Damage in C6 and HT-22 Cell Lines

  • 期刊论文

  • 发表日期：

    2025年10月24日

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  • Beyza Nur Yerliyurt,
  • Ahmet Şevki Taşkıran,
  • Birnur Akkaya,
  • Recep Akkaya

摘要

In this study, the effect of Enoxaparin, a type of low molecular weight heparin (LMWH), on neuronal damage caused by pentylenetetrazol (PTZ)-induced epileptic seizures was investigated. The study utilized C6 and HT-22 cell lines, and the extent to which enoxaparin influenced cytotoxicity in these cells will be evaluated. For this purpose, four groups were established: a control group, a group exposed to PTZ, a group treated with enoxaparin, and a group treated with both PTZ and enoxaparin. Cell viability was measured using a 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2 H-tetrazolium-5-carboxanilide (XTT) assay. To evaluate the effects of enoxaparin administration on oxidative stress levels in cell lysates after PTZ-induced neuronal injury, total antioxidant (TAS) and total oxidant (TOS) levels were measured colorimetrically in both cell lines. Mouse nitric oxide (NO), neuronal nitric oxide synthase (nNOS) and rat inducible nitric oxide synthase (iNOS) commercial sandwich ELISA kits were used to measure the effects of enoxaparin on the nitric oxide pathway in cell lysates. As a result of normalization and evaluation of XTT data, it was observed that the viability rate of the group treated with PTZ only decreased to 60% in both cell lines. The results showed that PTZ caused cell damage by increasing oxidative stress and disrupting signaling in neurons. Enoxaparin treatment prevented cytotoxicity by increasing antioxidant capacity and exhibited a neuroprotective effect by suppressing the inflammatory response.